Page 63 - EJMO-9-3

Eurasian Journal of
Medicine and Oncology An update on SLE

central to SLE. They help autoreactive B-cells survive, 4.2. Mucocutaneous involvement
promote monocytes to differentiate into dendritic cells, Skin and mucous membrane lesions are common. The
and boost the expression of MHC class II molecules, which facial “butterfly rash,” a malar rash over the cheeks and
ramps up antigen presentation. The increased activity of nose, is a hallmark of SLE and is often triggered by sun
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IFN-inducible genes, known as the “IFN signature,” is a exposure. Some patients may develop discoid lesions,
hallmark of SLE and is closely tied to disease severity. 43 which can lead to scarring. Photosensitivity is a frequent
In addition to B-cell dysregulation, T-cell abnormalities characteristic. Oral and nasal ulcers are usually painless,
are also critical in the pathogenesis of SLE. Regulatory and non-scarring alopecia is common. 50
T cells (Tregs), which normally keep autoimmune
responses in check, are often reduced in number or do not 4.3. Cardiac and vascular involvement
function appropriately in SLE patients. Making matters Pericarditis is a common cardiac manifestation of SLE,
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worse, there is an increase in T-helper 17 (Th17) cells, affecting about 25% of patients. Other cardiac issues
which produce the inflammatory cytokine interleukin include myocarditis, an increased risk of coronary artery
(IL)-17. This contributes to the chronic inflammation disease, and the potential for valvular disease due to
that is a hallmark of SLE. The imbalance between Libman-Sacks endocarditis. Raynaud phenomenon
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50
Tregs and Th17 cells further disrupts the body’s ability occurs in up to 50% of patients, presenting as cold-induced
to maintain self-tolerance, allowing the autoimmune acral pallor followed by cyanosis. Vasculitis occurs in 11
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response to continue unabated. Furthermore, the – 36% of patients, often manifesting as cutaneous lesions,
chronic activation of the immune system in SLE leads although larger vessels can also be involved. 52
to widespread tissue damage and organ dysfunction,
with the kidneys, skin, joints, and central nervous 4.4. Thromboembolic disease
system being particularly susceptible. Advances in Thromboembolic events, including arterial and venous
understanding the underlying mechanisms of SLE have thrombi, complicate SLE, especially in patients with
paved the way for targeted therapies to modulate the antiphospholipid antibodies. In one study, 11% of patients
immune response, such as B-cell depletion strategies experienced arterial and 5% experienced venous events
and IFN inhibitors. However, the heterogeneous nature over a median follow-up of 6.3 years. 53
of the disease poses ongoing challenges in developing
universally effective treatments. The pathogenesis of 4.5. Kidney involvement
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SLE, therefore, represents a complex interplay of genetic, Lupus nephritis occurs in about 50% of patients and is a
environmental, hormonal, and immunological factors, significant cause of morbidity and mortality. It can present
each contributing to the initiation and perpetuation of as asymptomatic hematuria or more severe conditions,
the autoimmune process. such as nephrotic syndrome and rapidly progressive

4. The clinical manifestations of SLE glomerulonephritis. 54
Fatigue, fever, and weight loss are common in SLE. Fatigue 4.6. Gastrointestinal involvement
affects 80 – 100% of patients and is often associated with Gastrointestinal symptoms occur in 40% of patients and
depression, sleep disturbances, and fibromyalgia. Fever are often caused by medications or infections. Other SLE-
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occurs in over 50% of patients, but it is usually challenging related gastrointestinal issues can include esophagitis,
to distinguish lupus-related fever from other causes, such pancreatitis, and mesenteric vasculitis. 55
as infection or drug reactions. Lupus-related fever typically
responds to non-steroidal anti-inflammatory drugs, 4.7. Pulmonary involvement
acetaminophen, or glucocorticoids, whereas fever due Pulmonary manifestations include pleuritis, pneumonitis,
to infection may not. Weight changes are frequent and interstitial lung disease, and pulmonary hypertension.
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may result from SLE itself or its treatment; for example, Immunosuppressive therapy increases the risk of
glucocorticoid use may lead to weight gain, while decreased pulmonary infections. 56
appetite can cause weight loss (Figure 1).
4.8. Neurologic and neuropsychiatric involvement
4.1. Arthritis and arthralgias
Neurologic and psychiatric manifestations are diverse,
Over 90% of SLE patients experience arthritis or ranging from seizures and strokes to cognitive dysfunction
arthralgias. The arthritis is often migratory, polyarticular, and psychosis. Antiphospholipid antibodies and lupus
and symmetrical, affecting multiple joints without causing anticoagulants can increase the risk of thromboembolic
joint erosion or deformity, unlike rheumatoid arthritis. 49 events, leading to neurologic complications. 56

Volume 9 Issue 3 (2025) 55 doi: 10.36922/EJMO025090042